Evidence map›Paper›PMID 32917732›Full record

ArticleHeart (British Cardiac Society)2020

Dipeptidyl peptidase-4 inhibition to prevent progression of calcific aortic stenosis.

Sahmin Lee, Seung-Ah Lee, Bongkun Choi, Ye-Jee Kim, Soo Jin Oh, Hong-Mi Choi, Eun Kyoung Kim, Dae-Hee Kim, Goo-Yeong Cho, Jong-Min Song and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Heart (British Cardiac Society), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. ILK-Dependent Modulation of DPP4 Prevents Progression of Calcific Aortic Valve Disease.Arteriosclerosis, thrombosis, and vascular biology · 2026
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  13. DPP4 as a Potential Candidate in Cardiovascular Disease.Journal of inflammation research · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

Sahmin Lee *Division of Cardiology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Seung-Ah Lee *Division of Cardiology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.ORCID 0000-0001-6964-8356
Bongkun ChoiDepartment of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Ye-Jee KimDivision of Clinical Epidemiology and Biostatistics, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Soo Jin OhConvergence Medicine Research Center, Asan Institute for Life Sciences, Asan MedicalCenter, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Hong-Mi ChoiDivision of Cardiology, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam, Republic of Korea.
Eun Kyoung KimDivision of Cardiology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Dae-Hee KimDivision of Cardiology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Goo-Yeong ChoDivision of Cardiology, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam, Republic of Korea.ORCID 0000-0002-7067-5535
Jong-Min SongDivision of Cardiology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Seung Woo ParkDivision of Cardiology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Duk-Hyun KangDivision of Cardiology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Jae-Kwan SongDivision of Cardiology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea jksong@amc.seoul.kr.ORCID 0000-0002-6469-801X
Ulsan College · KRSamsung Medical Center · KRSeoul National University Bundang Hospital · KR

Funding

British Heart Foundation PG/19/40/34422
6 · The paper itself

Abstract

objectiveTo evaluate whether the use of dipeptidyl peptidase-4 (DPP-4) inhibitors and their cardiac tissue distribution profile and anticalcification abilities are associated with risk of aortic stenosis (AS) progression.

methodsOut of the five different classes of DPP-4 inhibitors, two had relatively favourable heart to plasma concentration ratios and anticalcification ability in murine and in vitro experiments and were thus categorised as 'favourable'. We reviewed the medical records of 212 patients (72±8 years, 111 men) with diabetes and mild-to-moderate AS who underwent echocardiographic follow-up and classified them into those who received favourable DPP-4 inhibitors (n=28, 13%), unfavourable DPP-4 inhibitors (n=69, 33%) and those who did not receive DPP-4 inhibitors (n=115, 54%).

resultsMaximal transaortic velocity (Vmax) increased from 2.9±0.3 to 3.5±0.7 m/s during follow-up (median, 3.7 years), and the changes were not different between DPP-4 users as a whole and non-users (p=0.143). However, the favourable group showed significantly lower Vmax increase than the unfavourable or non-user group (p=0.018). Severe AS progression was less frequent in the favourable group (7.1%) than in the unfavourable (29.0%; p=0.03) or the non-user (29.6%; p=0.01) group. In Cox regression analysis after adjusting for age, baseline renal function and AS severity, the favourable group showed a significantly lower risk of severe AS progression (HR 0.116, 95% CI 0.024 to 0.551, p=0.007).

conclusionsDPP-4 inhibitors with favourable pharmacokinetic and pharmacodynamic properties were associated with lower risk of AS progression. These results should be considered in the preparation of randomised clinical trials on the repositioning of DPP-4 inhibitors.

Indexed as

Dipeptidyl-Peptidase IV InhibitorsAgedAnimalsAortaAortic ValveAortic Valve StenosisBlood Flow VelocityCalcinosisDisease Models, AnimalDisease ProgressionDrug MonitoringEchocardiographyElectronic Health RecordsFemaleHumansMaleDipeptidyl-Peptidase IV Inhibitorsaortic stenosis

Identifiers

PMID32917732
PMCPMC7677484
OpenAlexW3085231253

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.